Study published in Nature suggests that diagnostic MIF genotyping may predict risk in patients with coronary artery disease.
Yale School of Medicine researchers report that the protein macrophage migration inhibitory factor (MIF) influences the heart’s response to a lack of oxygen and blood flow.
Previously, scientists showed that MIF regulates the immune response, contributing to hardening of the arteries, arthritis, and the body’s response to infection. The current study found that mice lacking the MIF gene had a deficient AMP-activated protein kinase (AMPK) response and suffered more severe heart attacks than mice with an intact MIF gene. AMPK is a cellular-stress response enzyme that regulates the cellular-energy balance and protects the heart from injury during a heart attack.
A common variation in the MIF gene also leads to lower levels of MIF protein expression. The study showed that cells from people with this genetic variant also have less activation of AMPK. “This suggests that we might be able to identify individuals based on their genetic characteristics who are likely to suffer more cardiac damage during a heart attack,” says senior author, Lawrence Young, M.D., professor of cardiovascular medicine and physiology.
The research group also notes that MIF modulates the activation of the cardioprotective AMPK pathway during ischaemia, functionally linking inflammation and metabolism in the heart.
The study is published in the January 31 issue of Nature.
